PMID- 28803836
OWN - NLM
STAT- MEDLINE
DCOM- 20170919
LR  - 20180212
IS  - 1096-0384 (Electronic)
IS  - 0003-9861 (Linking)
VI  - 631
DP  - 2017 Oct 1
TI  - Methionine sulfoxide reductase A protects against lipopolysaccharide-induced 
      septic shock via negative regulation of the proinflammatory responses.
PG  - 42-48
LID - S0003-9861(17)30327-2 [pii]
LID - 10.1016/j.abb.2017.08.008 [doi]
AB  - Methionine sulfoxide reductase A (MsrA) is a major antioxidant enzyme that 
      specifically catalyzes the reduction of methionine S-sulfoxide. In this study, we 
      used MsrA gene-knockout (MsrA(-/-)) mice and bone marrow-derived macrophages 
      (BMDMs) to investigate the role of MsrA in the regulation of inflammatory 
      responses induced by lipopolysaccharide (LPS). MsrA(-/-) mice were more 
      susceptible to LPS-induced lethal shock than wild-type (MsrA(+/+)) mice. Serum 
      levels of the proinflammatory cytokines IL-6 and TNF-alpha induced by LPS were higher 
      in MsrA(-/-) than in MsrA(+/+) mice. MsrA deficiency in the BMDMs also increased 
      the LPS-induced cytotoxicity as well as TNF-alpha level. Basal and LPS-induced 
      reactive oxygen species (ROS) levels were higher in MsrA(-/-) than in MsrA(+/+) 
      BMDMs. Phosphorylation levels of p38, JNK, and ERK were higher in MsrA(-/-) than 
      in MsrA(+/+) BMDMs in response to LPS, suggesting that MsrA deficiency increases 
      MAPK activation. Furthermore, MsrA deficiency increased the expression and 
      nuclear translocation of NF-kappaB and the expression of inducible nitric oxide 
      synthase, a target gene of NF-kappaB, in response to LPS. Taken together, our results 
      suggest that MsrA protects against LPS-induced septic shock, and negatively 
      regulates proinflammatory responses via inhibition of the ROS-MAPK-NF-kappaB 
      signaling pathways.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Singh, Mahendra Pratap
AU  - Singh MP
AD  - Department of Biochemistry and Molecular Biology, Yeungnam University College of 
      Medicine, Daegu, Republic of Korea; School of Bioengineering and Biosciences, 
      Department of Zoology, Lovely Professional University, Phagwara, 144411, Punjab, 
      India.
FAU - Kim, Ki Young
AU  - Kim KY
AD  - Department of Biochemistry and Molecular Biology, Yeungnam University College of 
      Medicine, Daegu, Republic of Korea.
FAU - Kwak, Geun-Hee
AU  - Kwak GH
AD  - Department of Biochemistry and Molecular Biology, Yeungnam University College of 
      Medicine, Daegu, Republic of Korea.
FAU - Baek, Suk-Hwan
AU  - Baek SH
AD  - Department of Biochemistry and Molecular Biology, Yeungnam University College of 
      Medicine, Daegu, Republic of Korea.
FAU - Kim, Hwa-Young
AU  - Kim HY
AD  - Department of Biochemistry and Molecular Biology, Yeungnam University College of 
      Medicine, Daegu, Republic of Korea. Electronic address: hykim@ynu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170810
PL  - United States
TA  - Arch Biochem Biophys
JT  - Archives of biochemistry and biophysics
JID - 0372430
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.8.4.- (Methionine Sulfoxide Reductases)
RN  - EC 1.8.4.11 (methionine sulfoxide reductase)
SB  - IM
MH  - Animals
MH  - Cytokines/immunology
MH  - Female
MH  - Gene Deletion
MH  - Inflammation/complications/genetics/*immunology
MH  - Inflammation Mediators/immunology
MH  - Lipopolysaccharides/*immunology
MH  - MAP Kinase Signaling System
MH  - Male
MH  - Methionine Sulfoxide Reductases/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/immunology
MH  - Reactive Oxygen Species/immunology
MH  - Shock, Septic/complications/genetics/*immunology
MH  - Signal Transduction
MH  - Tumor Necrosis Factor-alpha/immunology
OTO - NOTNLM
OT  - Immune response
OT  - Inflammation
OT  - Methionine sulfoxide
OT  - MsrA
OT  - Nuclear factor kappaB
EDAT- 2017/08/15 06:00
MHDA- 2017/09/20 06:00
CRDT- 2017/08/15 06:00
PHST- 2017/05/22 00:00 [received]
PHST- 2017/07/24 00:00 [revised]
PHST- 2017/08/09 00:00 [accepted]
PHST- 2017/08/15 06:00 [pubmed]
PHST- 2017/09/20 06:00 [medline]
PHST- 2017/08/15 06:00 [entrez]
AID - S0003-9861(17)30327-2 [pii]
AID - 10.1016/j.abb.2017.08.008 [doi]
PST - ppublish
SO  - Arch Biochem Biophys. 2017 Oct 1;631:42-48. doi: 10.1016/j.abb.2017.08.008. Epub 
      2017 Aug 10.